Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake

In Alzheimer's disease (AD), the impairment of declarative memory coincides with the accumulation of extracellular amyloid-β protein (Aβ) and intraneuronal tau aggregates. Dementia severity correlates with decreased synapse density in hippocampus and cortex. Although numerous studies show that...

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Veröffentlicht in:	Neuron (Cambridge, Mass.) Mass.), 2009-06, Vol.62 (6), p.788-801
Hauptverfasser:	Li, Shaomin, Hong, Soyon, Shepardson, Nina E., Walsh, Dominic M., Shankar, Ganesh M., Selkoe, Dennis
Format:	Artikel
Sprache:	eng
Schlagworte:	Amyloid beta-Peptides - pharmacology Animals Bicuculline - analogs & derivatives Bicuculline - pharmacology Biophysics Calcium - metabolism CELLBIO CHO Cells - metabolism Cricetinae Cricetulus Drug Interactions Electric Stimulation - methods Enzyme Inhibitors - pharmacology Excitatory Amino Acid Antagonists - pharmacology Extracellular Fluid - drug effects Extracellular Fluid - metabolism GABA Antagonists - pharmacology Gene Expression Regulation, Enzymologic - drug effects Glutamic Acid - metabolism Hippocampus - cytology Humans HUMDISEASE In Vitro Techniques Long-Term Synaptic Depression - drug effects Long-Term Synaptic Depression - physiology Mice MOLNEURO Neurons - drug effects Patch-Clamp Techniques - methods Peptide Fragments - pharmacology Ryanodine - pharmacology Signal Transduction - drug effects
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